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Erschienen in: Archives of Virology 12/2013

01.12.2013 | Original Article

MiR-199a-5p promotes migration and tube formation of human cytomegalovirus-infected endothelial cells through downregulation of SIRT1 and eNOS

verfasst von: Shanchao Zhang, Lei Liu, Ruijin Wang, Houzhen Tuo, Yanjun Guo, Li Yi, Jiawei Wang, Dexin Wang

Erschienen in: Archives of Virology | Ausgabe 12/2013

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Abstract

Human cytomegalovirus (HCMV) infection has been shown to contribute to vascular disease through the induction of angiogenesis. However, the role of microRNA in angiogenesis induced by HCMV infection remains unclear. The present study was thus designed to explore the potential effect of miR-199a-5p on angiogenesis and to investigate the underlying mechanism in endothelial cells. We found that HCMV infection of endothelial cells (ECs) enhanced expression of miR-199a-5p and reduced the SIRT1 protein level at 24 h postinfection (hpi). Transfection with miR-199a-5p mimics significantly suppressed SIRT1 protein expression and promoted cellular migration and tube formation induced by HCMV infection, which could be reversed by transfection with an miR-199a-5p inhibitor. Furthermore, pretreatment with resveratrol depressed motility and tube formation of HCMV-infected ECs, which could be reversed by SIRT1 siRNA. Finally, overexpression of miR-199a-5p decreased the level of eNOS modulated by SIRT1, an effect repressed by transfection with an miR-199a-5p inhibitor. In summary, HCMV infection of endothelial cells upregulates miR-199a-5p expression and enhances cell migration and tube formation through downregulation of SIRT1/eNOS by miR-199a-5p.
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Metadaten
Titel
MiR-199a-5p promotes migration and tube formation of human cytomegalovirus-infected endothelial cells through downregulation of SIRT1 and eNOS
verfasst von
Shanchao Zhang
Lei Liu
Ruijin Wang
Houzhen Tuo
Yanjun Guo
Li Yi
Jiawei Wang
Dexin Wang
Publikationsdatum
01.12.2013
Verlag
Springer Vienna
Erschienen in
Archives of Virology / Ausgabe 12/2013
Print ISSN: 0304-8608
Elektronische ISSN: 1432-8798
DOI
https://doi.org/10.1007/s00705-013-1744-1

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